Recent studies have confirmed that the peptide fractions derived from marine organisms exhibit good antioxidant and anti‐inflammatory activity, and oyster is an excellent nutrient resource with high‐protein content. In this study, the peptide fractions from oyster soft tissue were prepared after hydrolysis by pepsin (pH 2, 37°C), trypsin (pH 8, 37°C), and Maxipro PSP (pH 4.2, 50°C) with the optimized parameters (enzyme‐to‐substrate (E/S) ratio, 1:100 (w/w); hydrolysis time, 4 hr), respectively. Four fractions named as PEP‐1, PEP‐2, TRYP‐2, and MIX‐2 were obtained after separation with elution consisting of 20% or 40% ethanol. The MIX‐2 exhibited the highest hydrophobicity correlated well with its hydrophobic amino acid content, and TRYP‐2 exhibited much better antioxidant activity than other three elution samples. Furthermore, all of the bioactive peptide fractions were noncytotoxic and could selectively repress pro‐inflammatory mediators, TNF‐α, IL‐1β, IL‐6, and i‐NOS, at transcription level in RAW264.7 macrophage cells after LPS stimulation. The result suggests that the peptide fraction TRYP‐2 from oyster soft tissue hydrolysates might be a potential resource for natural anti‐inflammatory components.
Angiogenesis plays a critical role in the growth and metastasis of tumors, which makes it an attractive target for anti-tumor drug development. Deoxypodophyllotoxin (DPT), a natural product isolated from Anthriscus sylvestris, inhibits cell proliferation and migration in various cancer cell types. Our previous studies indicate that DPT possesses both anti-angiogenic and vascular-disrupting activities. Although the RhoA/ RhoA kinase (ROCK) signaling pathway is implicated in DPT-stimulated cytoskeleton remodeling and tumor vasculature suppressing, the detailed mechanisms by which DPT mediates these effects are poorly understood. In the current study, we found that DPT promotes cytoskeleton remodeling in human umbilical vein endothelial cells (HUVECs) via stimulation of AMP-activated protein kinase (AMPK) and that this effect is abolished by either treatment with a selective AMPK inhibitor or knockdown. Moreover, the cellular levels of LKB1, a kinase upstream of AMPK, were enhanced following DPT exposure. DPT-induced activation of AMPK in tumor vasculature effect was also verified by transgenic zebrafish (VEGFR2:GFP), Matrigel plug assay, and xenograft model in nude mice. The present findings may lay the groundwork for a novel therapeutic approach in treating cancer.
S-allyl-cysteine sulfoxide (alliin) is the main organosulfur component of garlic and its preparations. The present study aimed to examine the protective effect of alliin on cardiac function and the underlying mechanism in a mouse model of myocardial infarction (MI). Notably, alliin treatment preserved heart function, attenuated the area of infarction in the myocardium of mice and reduced lesions in the myocardium, including cardiomyocyte fibrosis and death. Further mechanistic experiments revealed that alliin inhibited necroptosis but promoted autophagy in vitro and in vivo. Cell viability assays showed that alliin dose-dependently reduced the necroptotic index and inhibited the expression of necroptosis-related receptor-interacting protein 1, receptor-interacting protein 3 and tumor necrosis factor receptor-associated factor 2, whereas the levels of Beclin 1 and microtubule-associated protein 1 light chain 3, which are associated with autophagy, exhibited an opposite trend upon treatment with alliin. In addition, the level of peroxisome proliferator-activated receptor γ was increased by alliin. Collectively, these findings demonstrate that alliin has the potential to protect cardiomyocytes from necroptosis following MI and that this protective effect occurs via the enhancement of autophagy.
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